1,721,101 research outputs found
Mucosal colonization of gastric endocrine tumors mimicking mixed neoplasms
Two cases of gastric tumors showing mixed composition of endocrine cell clusters and exocrine glands and originally diagnosed as mixed neoplasms are described. In both cases, the exocrine glandular component was restricted to the upper third of the neoplasms being consistently absent in areas of muscular wall invasion and, in case 2, in nodal metastases. These glands were in close anatomical contiguity with the glands of the overlying gastric mucosa or, in case 1, apparently derived from deep pouch-like invaginations of the mucosa. They showed either lack of dysplasia (case 1) or mild dysplasia (case 2) with a Ki67 proliferation index consistently lower than that of the intramucosal glands. The intratumoral glands presented intestinal metaplastic features confirmed by intense Cdx2 immunostaining that, conversely, was absent in the endocrine component of the tumors. The latter showed intense vesicular monoamine transporter 2 immunoreactivity consistent with its origin from the enterochromaffin-like cells of the gastric oxyntic mucosa. On the basis of these findings, it is proposed that the exocrine glands do not represent a true neoplastic component of the tumors. Although mucosal entrapment by the tumor cannot be ruled out, they more likely reflect a hitherto unrecognized mechanism of mucosal colonization of gastric endocrine tumors
Expression of p4eBP1 and pS6K, two translational regulators of m-TOR Pathway in Stage IIa Colorectal Cancer Patients
Gastric carcinoid in the absence of atrophic body gastritis and with low Ki67 index: a clinical challenge.
Gastric carcinoids (GCs) represent 23% of all digestive neuroendocrine tumors (NETs). They can be distinguished into three types: type I (in the presence of atrophic body gastritis, ABG), type II (in the presence of Zollinger-Ellison/multiple endocrine neoplasia type I syndrome), type III (sporadic carcinoids, without any background pathology). To describe a case of undetermined type of GCs in an Italian referral center for NETs and its prevalence among GCs during a 6-year period. In a case series of 16 GCs seen at our unit between 2007 and 2012, 14 (83.3%) patients had type I carcinoid and 1 patient (6.2%) had type III carcinoid. One patient did not accomplish to the actual classification criteria. This patient had a well-differentiated carcinoid with low Ki67, but multiple gastric biopsies performed at 3-year follow-up gastroscopies excluded the presence of ABG. The patient had fundic cystic polyps, suggesting long-term use of proton pump inhibitors, possibly associated with GCs. This case shows that a GC may occur in the absence of ABG and with low Ki67 index, making classification according to actual criteria difficult. Further studies are needed to better understand the occurrence of this particular type of GCs
CDX1 expression is reduced in colorectal carcinoma and is associated with promoter hypermethylation
The CDX1 homeobox gene encodes a transcription factor specifically expressed in normal intestinal and colonic epithelia, and CDX1 gene expression is affected during colorectal tumour progression. In this study, real-time quantitative RT-PCR was used to investigate CDX1 expression in 26 colorectal carcinomas. Reduced expression of CDX1 was observed in 19 of 26 colon carcinomas compared to matched normal colonic mucosa: the decrease in CDX1 expression ranged between 0.10 and 0.79 (21-90% decrease; mean 64.75% ±22; p = 0.001). Mutation and loss of heterozygosity (LOH) analyses were then used to determine if reduced CDX1 expression was due to genetic alteration. No CDX1 gene mutations, but two known polymorphisms in exon 1, were observed. LOH was observed in 33% of the tumours investigated but this was not related to CDX1 expression. Since aberrant promoter methylation is a well-known mechanism that participates in gene silencing, the methylation status of the CDX1 5′ CpG island promoter was also investigated. PCR amplification of bisulphite-treated DNA followed by cloning was performed in 7 carcinomas that showed low expression of CDX1 and in 1 colonic carcinoma without reduced expression. Promoter hypermethylation occurred in carcinomas in which CDX1 reduced expression was present. These results suggest that CDX1 promoter hypermethylation is one of the molecular mechanisms that accounts for reduced CDX1 gene expression in colorectal carcinoma. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd
Monocyte chemotactic protein-1 in the inflammatory pseudotumour of the lung
Aims-Monocyte chemotactic protein 1 (MCP-1) and interleukin 8 (IL-8) are small, inducible proteins with chemotactic activity for specific subsets of leucocytes. The possibility that MCP-I and IL-8 are produced in tissues involved by Hodgkin's disease, thus contributing to the inflammatory-type background of the lesion, was investigated.
Methods-The presence of RNA transcripts for MCP-1 and IL-8 was investigated in biopsy samples of 24 cases of Hodgkin's disease, 17 non-Hodgkin's malignant lymphomas, 30 solid tumours, and 30 histologically normal tissues by means of reverse transcription-polymerase chain reaction (RT-PCR) Southern blot analysis.
Results-MCP-l expression was detected in 23 of 24 cases of Hodgkin's disease, in seven of 17 cases of B cell non-Hodgkin's lymphoma, and in seven of 14 cases of reactive lymphoid hyperplasia. IL-8 was present in six of 14 cases of Hodgkin's disease, and was seen only rarely in B cell non-Hodgkin's lymphoma and in reactive lymphoid tissues. MCP-1 and IL-8 RNA transcripts were detected in 13 of 25 carcinomas originating from the lung, breast, thyroid, and ovary.
Conclusions-These findings are consistent with the possibility that MCP-1 and IL-8 are two additional cytokines involved in the pathogenesis of Hodgkin's diseas
Gd-EOB-DTPA-Enhanced magnetic resonance findings of a giant inflammatory hepatocellular adenoma. a case report and review of the literature
Hepatocellular adenoma (HCA) is a rare benign tumour mainly found in women who have been receiving oral contraceptives [1].
According to recent studies, HCAs are currently catego- rized in four distinct genetic and pathologic subtypes as fol- lows: inflammatory HCA, hepatocyte-nuclear-factor-1- alpha-(HNF-1α-mutated) HCA, β-catenin-mutated HCA and Bunclassified^ subtype [2, 3].
Inflammatory HCA is also known as telangiectatic HCA and previously referred to as telangiectatic focal nodular hy- perplasia (FNH) [4, 5]. This particular subtype of HCA has specifically been linked to an increased body mass index and a generalized systemic inflammatory condition [4, 6].
Magnetic resonance imaging (MRI) is now established as the method of choice to evaluate focal liver lesions [7, 8]; furthermore, thanks to the introduction of hepatobiliary con- trast agents, the possibility to characterize lesions is really improved [9, 10].
Gadobenate dimeglumine and gadoxetic acid disodium (Gd-EOB-DTPA) are hepatobiliary contrast agents currently available [11].
Gadoxetic acid disodium (gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid, Gd-EOB-DTPA, Primovist, Bayer HealthCare, Berlin, Germany) is an hepatobiliary MR contrast agent which offers the combined properties of an extracellular space contrast medium during the vascular-interstitial phases and a liver-specific agent, with an hepatobiliary phase at 20 min after intravenous contrast injection [12].
Recent studies highlight the significant role of Gd-EOB- DTPA-MRI in the diagnosis of hepatocellular carcinoma [13, 14] and suggest that MRI achieves the greatest accuracy in differentiating HCA from FNH with the introduction of liver hepatocyte-targeted contrast agents [15, 16].
However, the inflammatory HCA presents pathological features similar to FNH; in fact, this subtype of HCA can mimic FNH on Gd-EOB-DTPA-MRI [17].
We describe the case of a 22-year-old obese diabetic wom- an, on oral contraceptive therapy, who presents constant and intense upper abdominal pain as the main symptom of a large HCA. This case report was approved by our Institutional Re- view Board and patients’ informed consent was waived
Endoscopic diagnosis of gastric intestinal metaplasia in patients with autoimmune gastritis using narrow-band imaging. does pseudopyloric metaplasia muddy the waters?
Background and study aims In autoimmune atrophic gastritis (AAG), associated with intestinal (IM) and/or pseudopyloric metaplasia (PPM), endoscopic surveillance is recommended for gastric cancer risk mainly linked to IM. Endoscopic Grading of Gastric Intestinal Metaplasia (EGGIM) reliably identifies IM, but has not been assessed in AAG. We aimed to assess the performance of EGGIM (index test) versus histology (reference test) of corpus IM in AAG.
Patients and methods This was a cross-sectional study of 210 AAG patients undergoing surveillance gastroscopy with narrow-band imaging (NBI): corpus IM scored according to EGGIM, histology according to updated Sydney system, and morphological criteria.
Results NBI identified corpus IM in 88.6 % of AAG patients: EGGIM were 0, 1, 2, 3, 4 in 11.4 %, 0.5 %, 33.3 %, 1.9 %, and 52.9 %, respectively. Histology identified corpus IM in 78.1 % and PPM in 79.5 % of patients. PPM was present with IM in 57.6 % and without IM in 21.9 % patients, 20.5 % had IM without PPM. EGGIM, compared to histology, correctly classified 76.2 % of patients, showing high sensitivity (91.5 %, 95 %CI 86.1–95.3). EGGIM correctly classified 93 % of patients with IM without PPM, 90.9 % with both metaplasias, and 21.7 % with PPM without IM yielding low specificity (21.7 %, 95 %CI 10.9–36.4).
Conclusions In AAG, EGGIM showed high accuracy and sensitivity identifying > 90 % of patients with histological corpus IM. EGGIM overestimated IM when PPM without IM was present, yielding low specificity. These findings raise the question of whether in AAG, PPM and IM may display similar endoscopic features on NBI
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